在动脉样硬化中,LncRNA ZEB2-AS1调节ox-LDL诱导的血管内皮细胞功能障碍通过海绵 miR-149-5pp
Kun Zhang1, Wei Song2, Bing Liu1
1Department of Vascular Surgery, The Affiliated Hospital of Qingdao University, Qingdao, People's Republic of China.
Journal of biochemical and molecular toxicology
|February 5, 2026
概括
长非编码RNAZEB2-AS1在动脉样硬化 (AS) 中被上调,通过向miR-149-5p.p.来恶化内皮功能障碍. 这表明ZEB2-AS1是潜在的生物标志物和AS的治疗标.
科学领域:
- 心血管研究研究心血管研究
- 分子生物学分子生物学
- 遗传学 是一个遗传学.
背景情况:
- 内皮功能障碍是动脉样硬化 (AS) 的核心,这是一个主要的心血管疾病.
- 长非编码RNAs (lncRNAs) 在AS病变发生过程中发挥作用.
- 在AS相关的内皮功能障碍中ZEB2-AS1的特定作用需要阐明.
研究的目的:
- 在AS中调查lncRNA ZEB2-AS1的表达和诊断价值.
- 探索ZEB2-AS1对内皮细胞增殖和炎症的功能影响.
- 确定涉及AS中的ZEB2-AS1的潜在分子机制.
主要方法:
- 在AS患者和对照组中检测到ZEB2-AS1表达,通过GSE120521数据集进行验证.
- 使用牛-LDL诱导的HUVECs建立了体外AS模型,并执行了ZEB2-AS1敲击.
- 评估细胞活力 (CCK-8),炎症因子 (ELISA) 和预测/验证的目标miRNAs (miR-149-5p).
主要成果:
- 在AS患者的血液和组织中,ZEB2-AS1被显著上调.
- 镇压ZEB2-AS1缓解ox-LDL诱导的内皮细胞功能障碍,减少炎症和粘附分子表达.
- ZEB2-AS1的目标是miR-149-5p,它调解了观察到的效应.
结论:
- 上调的ZEB2-AS1通过miR-149-5p通路加剧了AS中ox-LDL诱导的内皮功能障碍.
- ZEB2-AS1显示出作为AS诊断生物标志物的潜力.
- 在AS治疗中,ZEB2-AS1是一个有前途的治疗标.
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